Download - pediatric convulsion
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convulsions in children
Prepared by:
ANCY ANTO
M.Sc. Nursing
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History...
3000 yrs ago ......Babylonians wrote
about the symptoms and causes of
epilepsy
caused by demons attacking the person
The word epilepsy is derived from the
Greek word for "attack’’
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Patron of epilepsy.........
St.valentine
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World epilepsy day
National epilepsy dayNovember 17
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Did you know that: Epilepsy is not a form of mental illness
Epilepsy can begin at any age from birth to
99+
Epilepsy can & does affect memory and
learning.
NOTHING should be put in the mouth of a
person having a seizure
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Medication does not stop all seizures .
Epilepsy is not contagious
The tongue cannot be swallowed during a
seizure
Most seizures are not medical emergencies
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Seizures...
It is a transient occurrence of signs and / or
symptoms resulting from abnormal excessive or
synchronous neuronal activity in the brain
A sudden paroxysmal electrical discharge from the
CNS resulting in involuntary motor, sensory or
autonomic disturbances with or without alteration
in sensorium
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Epilepsy....
Is a disorder of the brain characterised by an
enduring predisposition to generate seizures
& by the neurological cognitive, psychological
& social consequences.
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Epileptic syndrome..
Is a disorder that manifests one or more
specific types and a specific age of onset and
a specific prognosis.
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Disorders mimicking seizures...
Jitteriness Benign neonatal sleep myoclonus Breath holding spells Shuddering attacks Syncopal attacks Night terror pseudo seizures
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Provoked vs. Unprovoked seizures..
Provoked = occurs during the course of acute
illness
Common causes Febrile seizures Metabolic events (b. sugar <36mg/dl) Acute CNS infections Drug intoxification Head trauma
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Incidence
72-80 / 1lak under 9 yrs of age
46-83 / 1lak under 14 yrs of age
Prevalence
Seizure disorders: 360/100,000 (India, Saha
SP 2003).
350/1lak in India
Greater in neonatal period
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Classification of Epileptic Seizures.
Partial seizures: Simple partial (consciousness retained)
MotorSensoryAutonomicPsychic
Complex partial (consciousness impaired)Simple partial, followed by impaired consciousnessConsciousness impaired at onset
Partial seizures with secondary generalization
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Generalized seizures Absences
Typical Atypical
Generalized tonic clonic Tonic Clonic Myoclonic Atonic Infantile spasms
Unclassified seizures
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ILAE classificationSelf limited
Focal Generalised
Continuous
Classification of epilepsy syndromes
•Idiopathic-focal & general
•Familial
•Symptomatic
•reflex
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Common causes
Infection to the central nervous system
1. Acquired bacterial meningitis
tuberculus meningitis
aseptic
encephalitis
cerebral malaria
2. Intrauterine infections
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Post infectious or post vaccinal encephalopathy
Pertussis vaccination
Pan encephalitis
Post measles encephalopathy
Chickenpox encephalopathy
Disseminated encephalomyeolopathy
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Metabolic causes
Dehydration
Dyselectrolytemia
Acidosis/ alkalosis
Hypocalcaemia/ hypomagnesaemia
Inborn errors of metabolism
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Space occupying lesions in the brain
Neoplasm
Brain abscess
Tuberculoma
Cysticercosis
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Vascular
Arterio venous malformations
Intracranial thrombosis/ haemorrhage
Coagulopathies
Congenital malformations
Migration defects
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Miscellaneous
Birth trauma
Birth asphyxia
Heat stroke
Brain swelling
Poisoning
Lead encephalopathy
Breath holding spells
Gray matter degeneration
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Drugs and poisons
Toxic doses of phenothiazine
Salicylate
Diphenylhydantoin
Carbon monoxide
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Causes
Early neonatal
period
Neonatal period 1m - 3 yrs
Birth asphyxia
Obstructed labour
IVH
Hypoglycaemia
IEM
Hypocalcaemia
Kernicterus
Developmental
malformations
Meningitis
Metabolic errors
Febrile
convulsions
Neurologic
infections
Metabolic causes
Lesions
drugs
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Mechanisms of seizure
1. Underlying aetiology
2. Epileptogenesis
3. Excitability
4. Neuronal injury after prolonged febrile &
afebrile status epilepticus
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Neuron – action potential
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Basic mechanisms of epileptogenesis
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Neurophysiology and neurochemistry
Epileptogenic neurons + disinhibition + circuit
PDS trigger Ca channel (Mg)
synchronization
Opens sp. K+ channel
Hyperpolarisation
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Hyperpolarisation
Disappear depolarisation
seizure
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Kindling
Process by which brief trans of electrical
stimuli are repeatedly delivered at
appropriate intervals to a susceptible area of
brain.
Prolonged generalised seizure
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Factors determine focal – generalised
Excitability of epileptic neurone
The ease with which the electric discharge
can be propagated from focus
Threshold of brain stem for disseminating an
electrical discharge
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Excitatory & inhibitory neurotransmitters
Glutamate & aspartate – Excitatory neurotransmitters
Induces Ca + ion current
Depolarisation
seizure
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Inhibitory neurotransmitters
GABA Hyperpolarisation
GABA receptors are coupled with Cl- channel
stabilises cell in
resting potential
Pyridoxine deficiency
Adenosine- inhibit the release of excitatory
neurotransmitters
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Catecholamine's & indolamines
↓ in nor epinephrine -↑ seizure susceptibility
↑ in nor epinephrine- ↓ seizure severity
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Biochemical alterations induced by seizure
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epilepsy syncope
Precipitating factors
Occurrence
Onset
Duration
Jerking limbs
Facial colour
Perspiration
Post ictal recovery
Post ictal confusion
EEG & prolactin
Rare
Awake , sleep
Abrupt
60-90 sec
Yes
Flushed
Hot, sweaty
Slow
Common
Positive
Common
Awake
Gradual
10-15 sec
Occasional
Pale
Cold, clammy
Rapid
Uncommon
Negative
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Partial seizures. Simple partial
Localised motor symptoms
Somatosensory, psychic, autonomic symptoms
Manifestations
- aversive seizure- eyes and head turn away
from focus & loss of consciousness
- rolandic seizure - tonic–clonic movements
involving face, salivation, arrested speech
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Jacksonian march- Sequential progression of Clonic movements
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Simple partial seizures with sensory signs.. Numbness
Tingling
Pricking
Paresthesia/ pain originating in one area
Visual sensations
Motor phenomena – posturing / hypertonia
- Uncommon < 8yrs
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Complex partial seizures(psychomotor seizures)
3yrs – adolescence
Characterised by - Period of altered behaviour- Amnesia- Inability to respond to environment- Impaired consciousness during event- Drowsiness / sleep- Confusion & amnesia
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aura
odd or pleasant odours
Auditory or visual hallucinations
Ill defined feelings (de javu)
Strong feelings of fear and anxiety
In small children
- emission of cry
- attempt to run
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Patterns of motor behaviour
Stereotypic
May suddenly cease activity , appear dazed
stare into space
Confused & apathetic
Become limp or stiff
automatisms
Post ictal confusion
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Exhibit oropharyngeal activities –smacking
chewing , drooling etc
Rarely exhibit – temper tantrums or rage
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Generalised seizures
Tonic clonic seizures (grandmal )
- Most common
- Occur without warning
Tonic phase clonic phase post ictal phase
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Tonic phase 10- 20 sec
Eyes roll upward
Immediate loss of consciousness
Stiffness
Contraction of entire body
Arms flexed
Legs, head & neck
flexed
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May utter a peculiar cry
Apnoeic
Increased salivation
Loss of swallowing reflex
If standing, falls to floor or ground
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Clonic phase
30 sec
Violent jerking movements
Foams at mouth
Incontinent of urine and faeces
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Post ictal state
Appears relaxed
Remain semiconscious
May awake in few minutes
Confused for several hours
Poor coordination
Mild impairment in fine motor movements
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Visual & speech difficulties
Vomit or complain of severe headache
Usually sleeps for several hours
Feels tired
No recollection of event
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Absence seizures (petit mal/ lapses) 4-12 years of age
common in girls than boys
Ceases at puberty
Brief / no loss of consciousness
No alteration in muscle tone
May go unrecognised
Abrupt in onset
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Manifestations:
Brief loss of consciousness
Without aura
5-10 sec
Slight loss of muscle tone
Minor movements
No incontinence
Amnesia
Need reorientation
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Atonic & akinetic seizures (drop attacks )
2-5 yrs
Sudden momentary loss of muscle tone &
postural control
Recurrent frequently
Manifestation :
- Loss of tone causing child to fall down
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Myoclonic seizures
Seizure episodes
Sudden brief contractions of a muscle
No post ictal state
May / not LOC
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Infantile spasms
Infantile myoclonus / massive spasms /
hypsarrhythmia / salaam episodes / Infantile
myoclonic spasms
6- 8 months of life
Twice common in boys
Numerous without post ictal drowsiness
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Manifestations
Series of sudden muscular contractons
Head flexed arms extended & legs drawn up
Eyes rolling
Preceded / followed by cry
May / not LOC
Flushing / pallor / cyanosis
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Jack-knife seizure – sudden dropping forward
of the head & neck with trunk flexed forward
Single momentary shock like contractions
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Comparison of simple, complex partial & absence seizure
Clinical features Simple complex Absence
Age of onset Any age Uncommon before 3 yrs
Uncommon before 3 yrs
Freq /day Variable 1- 2 times Multiple
Duration < 30 sec >60 sec <10 sec
Aura May be sole manifestation
Frequently never
Impaired consciousness
Never always Always
Automatisms never frequent frequent
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Clinical features
Simple complex Absence
Clonic movements
Frequent Occasional Occasional
Post ictal impairment
Rare Frequent Never
Mental disorientation
Rare Common Unusual
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Video game related epilepsy
Flicker frequency of video games
Type – generalised , simple / complex /
absence
Treatment – abstain from video games
Factors – screen brightness, sleep
deprivation, fatigue, fever, short distance from
screen
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Epilepsy syndromes
The Major Benign Partial Syndromes
1. Benign Rolandic Epilepsy
- Male preponderance 60%
- Onset 2 - 13 years (peak: 9-10 years)
- Older children- motor & somatosensory
symptoms, usually nocturnal.
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Younger children- Hemiclonic / GTCS
(especially at night).
Rx: None if seizures are mild and rare.
Most AEDs very effective.
Evolution: Recovery before 15 - 16 years.
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Benign Occipital Epilepsy
Frequency- rare
Genetic 37%, migraine 17%
Male = female
Onset 2 - 17 years (peak:7 - 8 years)
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Initial visual symptoms, often followed by a
hemiclonic seizure or by automatism
Postictal migrainous cephalgia in a quarter of
the cases.
Rx: Most AEDs with control in 60%.
Recovery by end of adolescence.
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The Major Primary Generalized Syndromes
Childhood Absence Epilepsy (True Petit Mal
Epilepsy)
Frequency 8%
Genetic predisposition- strong 20%
Female preponderance 75%
Onset 3 - 12 years (peak: 6 - 7 years)
Very frequent simple absences.
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Rx: VPA or ESM with control in 70 - 80%.
Evolution: Remission- 95%.
- Rare persistence of absences only- 6%.
- GTCS during adolescence or later- 40%.
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Juvenile Myoclonic Epilepsy (JME) Frequency 5%
Genetic predisposition- strong >25%
Male = female
Onset: 8-26 years (peak: 16 - 17) Myoclonus , GTCS often also occur,
occasionally absence. Rx: VPA with control in 60 - 100% Evolution: Rarely remits (<10%)
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Grand Mal on Awakening (GMA) Genetic predisposition- strong >10%
Male > female
Onset 6-24 (peak: puberty)
GTS exclusively or predoninantly (90%)
Myoclonic or absence may occur.
Rx: VPA with control in 60 - 100%
Evolution: Rarely remits (<20%)
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The Major Secondary Generalized Syndromes
Infantile Spasms (West Syndrome)
Lennox Gastaut Syndrome (LGS)
Frequency 3 - 10%
Genetic predisposition- no
Male preponderance
Onset 1 - 8 years (peak: 3 - 5 years)
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Poor prognosis in most cases
Tonic, atypical absence, drop attacks, other
generalized or partial seizures.
Rx: VPA,rarely with complete control.
persisting seizures.
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DIAGNOSTIC EVALUATION
History collection
Physical examination
Laboratory investigations
- Serum glucose & calcium levels
• Lumbar puncture – Ist febrile seizures
protein content – increased
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Imaging studies:
CT
MRI- structural lesions
PET-demonstrate perfusion,O2 & glucose intake
SPECT scan- perfusion in ictal & inter ictal state
Cerebral angiography
Magneto encephalography
Telemetry
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Electroencephalogram
Electric activity of brain.
Fast activity – beta rhythm(14 - 20 Hz)
Alpha rhythm – 8 -13 Hz
Theta rhythm – 4 - 7 Hz
Slow rhythm- 1 - 3 Hz
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Absence seizure
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Abnormalities.
Slow/ abnormal rhythm-generalised ,localised
or lateralised to one side thus helps to
anatomic lesions
Spikes
Sharp waves
Poly spikes
Slow waves (hypsarrhythmia)
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Tests consider in the evaluation of patients with seizures
Type Test Comments
Simple partial
Complex partial
GTC
Absences
MRI
MRI
MRI
None required
Rule out structural lesions Rule out structural lesions Rule out structural lesions
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Management of child with seizures
Goals:
1. Ensure adequate vitals & oxygenation
2. Terminate seizure activity
3. Prevent seizure recurrence
4. Establish the diagnosis & treat the
underlying
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steps
Step I – confirm diagnosis
Step II – establish seizure type & syndrome
Step III – evaluate the need for treatment
Step IV – select AED
Step V – start monotherapy (start slow go
slow policy) Step VI – switch to another monotherapy
add on therapy
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Treatment of a newly diagnosed case of epilepsy
Newly diagnosed case
Ist monotherarpy seizure therapy
IInd monotherapy/ combination therapy seizure
free
Intractable epilepsy
Combination therapy ketogenic diet , VNS
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Choice of AEDSeizure First line second line
partial CBZ, PHT, SVA , PB OXC, LTG, TPM
2nd gen GTCS SVA, ESM, CZP, CLB
LTG , TPM , LEV
GTCS SVA, CBZ, PHT, PB TPM, LTG, OXC, LEV
Absence SVA, CZP, CLB LTG , TPM , LEV
Myoclonic SVA LTG , TPM , LEV
Atonic / tonic SVA CBZ, CLB , NTZ, LTG, TPM
mixed SVA
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ILAE GUIDELINE FOR DRUG LEVEL MONITORING
Check compliance once or twice YEARLY
Suspect toxicity after each AED change
DURATION:
Withdrawal – if seizure free for 2 YEARS
Gradually over 6-12 wks
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Ketogenic diet
A very strict diet that involves fluid restriction,
high fat and low carbohydrate + protein
intake.
The goal: alter the body’s fuel source from
glucose to fat.
The basis of the diet – fasting
The encounter with a faith healer
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Duration – 2yrs
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Sample Meals:
Meal 1:
melted butter
heavy whipping
cream
chicken
apple
sugar free Jell-O
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Problems that may arise:
Low blood sugar
Lethargy
Nausea
Vomiting
Elevated cholesterol
Kidney stones
Constipation
Weight loss or gain
Dehydration
Cheating
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Vagus nerve stimulation
>12 years
50% reduction in
seizures
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Types of surgery
1. Resection
Removal of the area causing the seizures
2. Disconnection
Corpus callosotomy
Multiple subpial transections
3.Hemispherectomy
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procedure Type
Temporal lobectomy
nonTemporal lobectomy
Corpus callostomy
Hemispherectomy
Simple/ complex partial
Partial
Partial, tonic ,clonic
Unilateral , partial , hemiparesis
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Nursing management
Seizure precautions Relieving anxiety Managing treatment Providing family support & education
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Febrile seizures
Occurrence of seizure activity in
neurologically healthy infants & children
between 6 months & 5 yrs of age associated
with fever >38c without evidence of
intracranial infection & with no history of prior
afebrile seizures
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Common in 18- 22 months
Provoked seizures
Causes:
- Infections of middle ear
- URTI
- Urinary tract & GI infections
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Types
Simple febrile seizures:
- 85%
- Generalised seizures
- Lasting less than 15 min
- No post ictal neurologic abnormalities
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Complex febrile seizures
- Recurrent within 24 hrs
Febrile status
- A seizure with duration of 30 min
- Without regaining consciousness interictally
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Risk factors
Age <18 months
Family history
Shorter duration
Recurrence
75% within 1 yr
Risk of subsequent epilepsy – 2- 2.5 %
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Diagnostic evaluation
History
Serum electrolytes – calcium , magnesium
Blood glucose
LUMBAR PUNCTURE
abnormal neurological examination
Ongoing seizure
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Management
During the seizure
- Manage as for any other acute seizure
- Should hospitalise
o Lethargy
o Complex features
o Unclear follow up
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Long term management
Primary goal – to prevent recurrences
Antipyretics – to reduce fever
INTERMITTENT PROPHYLAXIS
Diazepam – 0.3 – 0.5 mg/ kg orally / rectally
clobazem - 1mg /kg / day
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Continuous prophylaxis
Indications :
- Recurrent complex seizures
- Abnormal neurodevelopment
- Positive family history
Sodium valproate is preferred
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Status epilepticus
A seizure that persists for a sufficient length
of time / is repeated frequently enough that
recovery between attacks does not occur
Early status established status
Epilepticus Epilepticus
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A condition characterised by an epileptic
seizure that is sufficiently prolonged or
repeated at sufficiently brief intervals so as to
produce an unvarying and enduring epileptic
condition
(dictionary of epilepsy )
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Etiology
Recurrent neonatal seizures
Traumatic subarachnoid haemorrhage
HIE
IEM
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Classification
Generalised status epilepticus
Partial status epilepticus
Refractory status epilepticus
Super refractory status epilepticus
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Generalised status epilepticus
Convulsive seizures
1. Tonic clonic
2. Tonic
3. Clonic
4. Myoclonic
Non convulsive
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Refractory status epilepticus
Persistent seizure beyond 120 min
Despite of therapy with benzodiazepine,
phenytoin, phenobarbitone or valproate
Treatment :- Midazolam - Thiopentone - Magnesium- Ketogenic diet
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Intractable epilepsy
It is defined as an at least one seizure every
2 months for the first 5 years of treatment &
subsequently as at least one seizure per year
with failure of at least 3 Ist line AEDs
Rx: surgery
Ketogenic diet
VNS
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Misconceptions about childhood epilepsy
Children with epilepsy are brain injured
Has mental handicaps
Only SE will harm child's brain
An EEG will determine if child has epilepsy
Abnormal EEG -↑ AED dose
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Child has twitches of legs & arms while
asleep. Are these seizures ?
Blood level AED ↑ - change the dose ?
AED – only way of treatment
Surgery – after a attempting all AED
Life will never be the same
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Nursing diagnosis
Risk for injury related to CNS dysfunction &
inability to control self secondary to the type of
seizure.
Risk for aspiration & ineffective breathing
pattern related to impaired motor activity, LOC.
Risk for injury related to impaired
consciousness & automatisms
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Anxiety / fear related to child having life
threatening seizure activity
Ineffective tissue perfusion
Interrupted family processes
Self esteem disturbances
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